INmune Bio Inc (INMB) 2020 Q1 法說會逐字稿

Greetings, and welcome to INmune Bio's First Quarter 2020 Earnings Call. (Operator Instructions) As a reminder, this conference is being recorded. A transcript will follow within 24 hours of this conference call.

At this time, it is my pleasure to introduce Mr. David Moss, Co-Founder and CFO of INmune Bio. David, the floor is yours.

Thank you, Latanya, and good afternoon, everybody. We thank you for joining us for the call for INmune Bio's First Quarter 2020 Financial Results Call. With me on the call is RJ Tesi, CEO and also Co-founder of INmune Bio, who will provide a business update.

Before we begin, I remind everyone that except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the safe harbor provision of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements. Please see the forward-looking statements disclaimer on the company's earnings press release as well as risk factors in the company's SEC filings, including our most recent quarterly filing with the SEC.

There is no assurance of any specific outcome. Undue reliance should not be placed on forward-looking statements, which speak only as of the date they are made as the facts and circumstances underlying these forward-looking statements may change. Except as required by law, INmune Bio disclaims any obligations to update these forward-looking statements to reflect future information, events or circumstances.

Now I'd like to turn the call over to RJ Tesi, CEO of INmune Bio. RJ.

Thank you, David, and thanks, everyone, for joining the call in these difficult times. Difficult and interesting, I think, is the best way to describe them. I will arrange my remarks to highlight key takeaways for the first quarter, the year-to-date and provide updates from our 2 platforms. Then I will turn it back to David Moss to discuss our financial results, upcoming milestones before we open the lines for Q&A.

We'll start with the DN-TNF platform. We have 4 therapeutic programs in development. These include INB03 for cancer, LIVNat for NASH, we have a new program that we're calling Quellor for treatment of cytokine storm related to COVID-19, and XPro1595 for Alzheimer's disease. I'll remind you that these are all the same drug from a single platform.

I'll start with our newest program with Quellor targeting cytokine storm to treat the complications of COVID-19. We initiated this program after completing a strategic assessment, and we are planning clinical trials with the DN-TNF platform for the treatment of the complications of this disease.

Our decision is based on the 4 TNF-related attributes of COVID-19 and the pathophysiology of the disease. The first is cytokine storm. This is, shall we say, a top line problem with COVID-19 and blunting the effects of the cytokine storm makes sense. Soluble TNF is a major part of the cytokine storm, and neutralizing soluble TNF is what DN-TNF platform does.

But the soluble TNF plays 2 other very important roles that are not as obvious to many. The first is that for tissue destruction to occur, immune cells must move from inside the blood vessel to outside the blood vessel and into the tissue where they cause the damage. Soluble TNF when it activates endothelial cells cause them to upregulate ICAM-1 and VCAM-1. These proteins are sort of like traffic cops that signal to activated immune cells that are living by in the bloodstream and signal them to stop and exit the blood vessel, it's called trafficking, into the tissue where they cause damage.

A more obscure role of soluble TNF is that it contributes to the coagulopathy, which is the cause of many of the complications related to the vexing disease. When soluble TNF activates endothelial cells and macrophages, they upregulate tissue factor. Tissue factor actually starts the coagulation cascade that results in much of the pathology associated with pulmonary, renal and vascular disease and probably neurologic disease.

In patients, this coagulopathy is heralded by elevated D-dimer, a biomarker of severe disease and present in almost every -- elevated in almost every patient who is admitted to the hospital. Working with clinicians and the regulatory authorities, we are moving rapidly to start a clinical trial that will attempt to prevent the catastrophic complications of COVID-19, including the need for mechanical ventilation. We hope to be enrolling patients by July, ideally in a program supported by nondilutive funding.

XPro is being used -- XPro1595 is being used to treat Alzheimer's disease, an apt metaphor for this program is steady as she goes. We are confident in our goal to have data for review in October, if not sooner. And we are beginning to plan for the Phase II trial, but we admit the pandemic has forced us to be creative.

Future programs must require fewer trips to the clinic without sacrificing the ability to collect critical data or the quality of that data. We have some ideas, we're working to implement them, and we'll tell you more about these in the future.

INB03, our cancer program is being targeted to treat women with metastatic HER2-positive breast cancer, especially those with CNS mets. Just a couple of weeks ago, we announced publication of an invited review in Frontiers of Oncology, entitled tumor necrosis factor, an opportunity to tackle breast cancer by Roxana Schillaci. She is the lead -- shall we say, thought leader that has been working with us on the role of TNF in cancers, especially breast cancer. And this publication is part of an evolving body of work by Dr. Schillaci and her team on the role of soluble TNF in resistance to immunotherapies, including trastuzumab and the tyrosine kinase inhibitors.

Just 3 days ago, Sophi Bruni, a doctoral student in Dr. Schillaci's lab presented work at the New York Academy of Science frontiers and immunotherapy 2020 meeting. That work demonstrated that combination of Lapatinib, a TKI inhibitor, and then INB03 overcomes resistance to trastuzumab in HER2-positive breast cancer models. This work informs the design of our planned Phase II trial in woman with brain mets from HER2-positive breast cancer.

Lapatinib is a dual EGFR HER2 inhibitor. It's part of the TKI class. It's a good drug in a difficult disease that suffers from early resistance. We believe we have identified this resistant mechanism, and we are targeting women with HER2-positive brain mets because both drugs cross the blood-brain barrier. All of these or most of these women will also be expressing MUC4, which makes them resistant to trastuzumab-based therapies.

Finally, the combination increases -- decreases myeloid-derived suppressor cells and the key immunosuppressive cells with the tumor microenvironment and makes cold tumors hot in animal models, and we hope this sets up this combination to be part of triple therapy that will include immune checkpoint inhibitors.

Just as an aside, tomorrow, AACR will be releasing their abstracts. This work is also being presented at the AACR. Originally, that was supposed to be the first release of the data. But as with many programs, COVID-19 has changed the calendar.

Moving to LIVNate for NASH. Giving patients new livers was a big part of my previous life as a transplant surgeon. But there's a surgical saying that says the sign of a good surgeon is the one who can avoid an operation. And that is the goal of this therapy to avoid the need for liver transplant.

We have identified a novel mechanism, pathologic mechanism to treat NASH. We believe that LIVNate seals the intestinal leak that is critical in driving inflammation in the liver. The leaky gut results in very high inflammatory cytokine load in the portal vein, 2 logs greater than what you'd see in the blood.

The portal vein feeds blood directly from the intestinal track into the liver, and this highly inflamed liquor has predictable effects on liver with inflammation, decreased hepatocyte survival, which ends up with fibrosis and changes in the liver histology.

The protocol is written, sites are identified. But we are delaying the initiation of this trial for now. Starting new trials in the COVID-19 era is challenging, starting trials in a disease that is not life-threatening is a bigger challenge, and as we ramp up the COVID-19 effort, we are husbanding our drug supply with our existing programs.

We have drug available to complete the Alzheimer's program to complete the planned COVID-19 program and to support -- but to support our expanding clinical programs, we have signed an agreement with KBI Biopharma to produce additional drug. This concludes my comments on the DN-TNF program, and I'll move to the NK-priming platform.

The NK-priming platform we call INKmune, and we have 2 therapeutic programs in the queue. INKmune will be studied in solid tumor and hematologic malignancies, ovarian cancer and high-risk MDS, respectively. The latter is a form of a pre-leukemia.

In April, we announced that the USPTO had provided formal notice of the allowance of a patent application, entitled in-vivo priming of natural killer cells. This is the first of several that are coming for this platform. The patent relates to, and I quote, "The method of treating cancer by administering a proprietary inactivated cellular material preparation and contacting a patient's own natural killer cells within the body to induce an in-vivo response, namely the priming of NK cells from enhancing the innate immune response and the NK cell ability to recognize it and kill cancer cells in the patient."

I'll remind you, we do not give new NK cells. We believe, and we have excellent data that support it, the petition saying the cancer patient NK cells are fine. They have all the tools they need to kill cancer cells, but they need targeting assistance. They need to be turned on, and that's what INKmune does.

The newly allowed patent is expected to issue in approximately 60 days and will expire in 2036. This is just, as I said, one of the many of the company's IP or patents that are -- we're expanding our portfolio, and we believe our patent portfolio is one of our finest assets.

The Phase I clinical programs in INKmune are being run in the U.K. The U.K. is suffering mightily from the COVID-19 pandemic, as are we. And both programs have been somewhat delayed by the fact that they aren't allowing clinical trials to move forward because of the pressures on the hospital.

We are cautiously optimistic that we can meet our goal to treat a patient in the high-risk MDS program by the end of the year. Realistically, we do not expect to treat a patient in the INKmune ovarian cancer trial until the first half of 2021.

So with that, I will turn it over to David, who will talk about our financial results and upcoming milestones.

Thank you, RJ. I'll provide a brief overview of our financial results and upcoming milestones. Net loss attributable to common stockholders for the first quarter ended March 31, 2020, was $2.1 million compared to $1.9 million for the quarter ended March 31, 2019.

Research and development expenses totaled approximately $0.8 million for the first quarter ended March 31, 2020, compared with approximately $0.6 million for the quarter ended March 31, 2019. General and administrative expense was approximately $1.3 million in each of the quarters ended March 31, 2020, and March 31, 2019.

At March 31, 2020, the company had cash and cash equivalents of approximately $5.9 million with no debt. As of May 13, 2020, the company had approximately 10.8 million shares outstanding.

Now I'd like to list our upcoming catalysts. To reiterate what we have detailed in our press release, some of the milestone time lines have been updated due to the ongoing COVID-19 pandemic, as RJ just spoke about.

First, we expect to report the results of the ongoing Phase I XPro1595 trial in Alzheimer's disease, expected to be completed in the second half of 2020 and have data in October, possibly sooner.

Second, we expect to submit an IND for Quellor for the prevention of pulmonary complications of COVID-19 infection this month 2020 or very early next month. Moreover, we are working to enroll the first patient in a Phase II Quellor program as soon as possible.

Third, we expect to enroll the first patient in the Phase II INB03 program targeting trastuzumab -- trastuzumab-resistant HER2-positive breast cancer using in INB03 as part of combination therapy in mid-2021.

Fourth, we expect to enroll the first patient in Phase II LIVNate for NASH in mid-2021.

Fifth, we expect to enroll the first patient in Phase I INKmune, high-risk MDS cancer by the end of this year and the second half of 2020.

Sixth, we expect to enroll the first patient in the Phase I INKmune program in ovarian cancer by mid-2021.

So as a small company, we have a lot of catalysts coming up. We remain very focused on meeting our milestones and delivering data and rewarding investors' faith and patience in the development of our business.

At this point, I'd like to thank you for your time and attention, and I'd like to turn it back to the operator for questions and answers. Latanya, can you please poll for questions?

(Operator Instructions) Our first question comes from Jonathan Aschoff with Roth Capital Partners.

I have 2 questions. The first is, since Lapatinib is the drug with which you intend to combine DN-TNF within Phase II, can't it be argued that, that drug has kind of already had its hay day, and therefore, maybe restoring Lapatinib sensitivity isn't as commercially exciting as restoring trastuzumab sensitivity? Do you want to discuss that a little?

Yes. That's a great question, Jonathan. The problem is, is that once it is -- if you get down to the way clinicians treat patients, once a patient has failed a drug that once they relapse, basically, on trastuzumab, which is what happens when a patient develops metastatic disease, particularly brain mets, they move on, right? And to argue to go to a -- it's a difficult discussion frequently to have with clinicians when they say -- to say, well, we can now -- if you give -- let's say you give Lapatinib with trastuzumab, the patient is going to respond, they get nervous about that.

But let's talk -- let's really take the next step. Obviously, there are a number of these trastuzumab drug conjugates out there now. And some of them have been -- have shown a bit of a signal in the brain. The problem is with the trastuzumab-based conjugate is if the patient is expressing MUC4, which almost all of these metastatic patients do, in fact, the trastuzumab can't bind with to.

So actually, trastuzumab resistance is actually a, shall we say, a biomarker for resistance to any trastuzumab-based strategy. So I think you're -- I think -- I actually think the future, and I'm speculating here is that I admit Lapatinib has -- maybe had its day in the sun, but it is indicated for the indication. And there are other TKIs, which show some -- that are newer that show some signal in these indications, I just don't have data with me.

I predict in the future, that we'll be combining ND03 with a number of TKIs because this may be a class effect. I don't know that yet. It may be. We are doing that research. But we have indications that, that might be the case. So I accept your comment, but it's hard to go against tradition. The tradition is once a clinician -- once a patient has progressed on a therapy, they move on.

Okay. What questions will be gear headed, can you help us, David, better understand the quarterly R&D expense trend over 2020, just looking at the drop from fourth Q to the first quarter?

I'm sorry, Jon, you want the R&D expense going forward?

Yes. Yes, just because there was such a big drop from the fourth quarter of '19 to the first quarter of '20.

I'll tell you what, we're currently evaluating the cost related to the COVID trial. It's somewhere -- the first part of the trial will be somewhere between $3 million to $5 million. We're not -- we're looking at nondilutive activity related to that. We're also looking at whether we can run -- what percentage of the trials we run in Australia, which allow us to get a rebate. I would like to take that off-line with you, if you don't mind, Jonathan, and have a call with you about that after this, if you don't mind.

Our next question comes from Jason McCarthy with Maxim.

Can you talk a little bit about the amount of drug product that you do have manufacture? You mentioned it earlier. And how much of that would be applicable to a COVID study? And for that COVID study, can you walk us through just a little bit of what you're thinking in terms of a trial size and maybe stage of disease? Would it be severe/ICU-insulated or something more mild to moderate or something in the middle, maybe in the hospitals, but not in the ICU just yet, just a little bit more clarity there.

And a question for David on the back end of that, would be, can you just elaborate a little bit on your relationship with KBI pharma? Because they are a great manufacturing partner. They support Coherus and a bunch of other names. Just talk a little bit about drug manufacturing with KBI.

Yes. So let me start. So we have more than enough drug to complete the COVID trial and the Alzheimer's trial. But we don't have enough drug to really jump into another trial that may have extensions. And what I mean by that when you set up a trial, for instance, of cancer patients, and if the patient is doing well on the therapy, the expectation as you carry them, you continue to treat them beyond the end of the trial. So we cannot make open-ended commitments.

The COVID trial is an interesting trial. When we talked to the FDA, we sent in one design, and they brought -- pushed back, actually, with a better design. They are asking us to do a 2-step Phase II trial that is they want 100-patient proof-of-concept that rolls right into a fully powered, for all practical purposes, pivotal trial that will allow us to really sit with the FDA and see what the next steps are.

The way we've designed it, so the 100 patients is a randomized, blinded trial, 1:1 randomization. It's follow-on trial with 260 patients, so a total of 360 patients will be treated 1:1 with that go/no-go decision after the first 100 patients.

The target patient is a patient who is admitted to the hospital with hypoxia, with room air sat less than 94% but not someone who's in the ICU. The purpose of the trial is to keep the patients out of the ICU. And the primary endpoint, and once again, this was dictated by the FDA, is respiratory failure. And we define respiratory failure as progression to mechanical ventilation, which is anything that has a ventilator with a plug attached to it.

So CPAP, BiPAP and traditional intubation with mechanical ventilation are the endpoints. And part of the reason is, as you know, there's been -- there's a really rapid change about how people are using intubation. People are using nonendotracheal tube forms of ventilation as long as they can, but our goal is to take a patient who comes in, may need oxygen support and keep them from sliding down that slippery slope.

We are very interested in the other pathologies with COVID-19. I mentioned the endothelial activation, which is, I think, underestimated in the disease. It is the cause of the coagulopathy, which contributes to the renal disease. It contributes to neurologic complications and is actually probably a big part of the problems before they develop the more traditional form of ARDS.

The patients we're treating will not have ARDS. It's not that we don't think the drug is a good drug for patients in ARDS. It's just that, that's, in my opinion, a different patient population. And we -- I'd rather keep -- now I've taken care of those patients. They are difficult patients. And I'd rather keep patients out of the ICU, off mechanical ventilation, than try to wrestle them once they've gone that far.

So I'll stop there and let David answer the question, and then let you respond, Jason.

So Jason, thanks for the question. Yes, we signed an agreement with KBI. They're a wonderful group. We've had a lot of discussions with them, and we have a very good consultant that we use as an intermediary to help us on the manufacturing front. We actually run this through our U.K. sub, so it's eligible for a rebate from the U.K. government.

It's somewhere between -- it will be a long-term relationship because if this goes well, obviously, we'll need to continually manufacture drugs as the programs expand. But the first part of the -- it's broken into really 2 different phases. And the first phase is really to do a pilot-scale manufacturing. And then the second phase is to do the clinical-grade material manufacturing.

We estimate it's about a 14- to 18-month-type period of agreement, could be accelerated, could be -- but it's a great arrangement that we have with them

Okay, great. And where would the trial be conducted? Would you be in Australia or someplace ex U.S. where you get rebates? I thought I recall, Australia was one of your sites.

Well, it was -- I tell you, I was interested because, as you know, we love the rebates, right? It's been a great source of nondilutive financing. But if you've been -- if you happen to, like I do, look at their Australian government website, they have done an extraordinary job of squashing the curve. I think 2 days ago, they had 80 patients in the hospital and 40 in the ICU, and that was on the whole continent, countrywide.

So this trial will be run primarily in the United States. And I will say one of the other areas we're very interested in, as you know, that blacks and Hispanics have a rough go with this disease, and there's a big debate about whether this is because that they have more of the comorbidities or if there's something else going on.

So I predict we will be running this in the centers or the parts of the country where the disease tidal wave is starting to hit. Places in the Mid South, Texas, the Southwest and the Southeast. And we plan and hope to have a patient population that looks a lot like the box, 1/3 Caucasian, 1/3 Hispanic and 1/3 black because when you're treating almost 400 patients, you can really learn a lot from them. But it will be...

Is the fall season coming in Australia, is that a possible factor for not having a few cases? Are you watching that? Or...

No, yes, we're watching that. But I think the problem, there's really a couple of issues there. One, what's happening there is about to start in an influenza season. So what's going to happen is the same thing that's going to happen here. As they begin to open up, they're going to have spots of disease, right? And they're going to see more cases than they see now.

But the question is, are they going to have the kind of intensity where you can pick 3 or 4 hospitals and pick up enough patients. It's a moving target, really, Jason. I am not ruling out having sites in Australia, but the trial will be driven for the most part, Assuming things work out with the IND and the FDA, the patient enrollment will really be driven out of the U.S.

Our next question comes from Michael Irwin with Univest Securities.

I actually have a few questions. So you said before that there was going to be some pushback of the trials for some of your plans of the current trial that was supposed to start later this year. Are there any -- you said before that you would release more data, but is there more information about the clinical design? Are there any plans of expediting the results for those trials to make up that 1-year delay?

Well, certainly, once we start the trial, the trial design is fixed. I mean, at the end of the day, as you know, what the limiting factor to almost every trial is speed of enrollment. So at this point, they are just being reset to move back to reflect the pandemic.

Okay. And then there's been news online about this complications with COVID-19 showing in pediatrics of a Kawasaki-like disease and are there any plans looking into those because there are some small links between TNF inhibitors and treatment options for Kawasaki disease.

Actually, we are -- thank you for that question. We are following them very closely. You are absolutely right. There is a role for -- a big role of TNF in the Kawasaki syndrome that -- in Kawasaki disease. And we expect that there's a similar role in this multisystem, this pediatric multisystem inflammatory disease, I believe that's the name.

So we've not yet seen anyone published cytokine data. We're looking for that very closely. We expect it's going to model what we see in Kawasaki disease. One of the things that the FDA made very clear in their response to us for a pre-IND and actually in the guidance they just released on Monday for clinical trials in COVID-19 is that you need a pediatric plan. And although they don't hold that -- hold you hostage to that plan, you have to have that planned very quickly.

Right now, we view that disease as our potential pediatric plan, I emphasize potential. We've not discussed it with the FDA yet, and we wait to get -- see some data to further support our interest. But once that -- our IND, assuming everything goes well, is open, and we start having follow-on discussions with the FDA. This is a disease that we think we have the perfect drug for because remember, it targets TNF, it targets endothelial cell activation, which is a big part of this disease, and it is not immunosuppressive. And one of the major differentiators of our anti-inflammatory strategy for many others out there is that we do not cause immunosuppression. In fact, we improve the immune response.

We have been -- if you give animal models that have bacterial infections or protozoal infections, they get better. We have tested this drug in models of Eastern equine encephalitis and Coxsackie B3 with the NIAID, and we did not make those animals worse. They did not die faster. We didn't make them get better either, but we did not -- they did not go worse.

So this drug is not immunosuppressive, which is an important consideration when you're treating people that have viral disease.

(Operator Instructions) Our next question comes from Arthur He with H.C. Wainwright.

This is Arthur for RK. Most of my questions being answered, I just have 2 -- maybe 2 quick ones. So first off, on your COVID-19 program, if I recalled correctly, you expect to start the trial in July. Could you give us more color on your expectations for the -- overall, the timing of the program?

Yes. So good question. So obviously, the calculation of July is, obviously, depends on the FDA. And I want to give -- I'm sure you've heard this from other companies. The FDA has been spectacular in dealing with the COVID-19 issue. They are quick in their responses. They're clear. They are here to help, which is often not the way it seems when you're a small biotech because they can be a rough taskmaster.

The rate of enrollment, obviously, would depend completely on where the disease is in the U.S. I think that anyone who thinks the disease is going to disappear in the summer, there are a few people that do, I'm not one of those people. As I mentioned earlier, I think it's going to roll across the South and the South Central and the Midwest. And then it's going to -- then in the fall, we're probably going to have secondary outbreaks where the first outbreaks are in the [wane], East Coast and the West Coast. I think it's going to be here for a while.

The current plan is that we're going to for the 100-patient go/no-go, is 5 to 7 sites, and the assumption is that they'll enroll at least one patient a week. So you can do the math. It's 100-patient randomized trial, 50 get drug and 50 don't get drug.

And by the way, Dave, I forgot to add -- talk about the way that the dosing, when Jason asked, but the -- and this is actually the FDA's recommendation, by the way. We designed it as a 2-dose study on a mission and 7 days later, and they pushed back and said make it a 1-dose study with a second dose if they are in the hospital. The expectation or the hope is that most of these patients actually leave the hospital by 7 days.

So to treat the 360 patients that we need to treat since only half of those 100 -- let's call it, 180 patients are getting treatment, then let's say, 20% get more than 2 doses, I mean 250 vials is all we need for this clinical trial, 350 dose -- or 250 doses. So that's a very -- it's a beautiful thing when you're a company doing a drug study where the drug supply is not a tremendous burden.

But anyway, Arthur, back to your question, our hope is the speed of which the trial enrolls is completely dependent on how severe the disease is. We will be placing our sites where we think the disease is going to be active this fall, this summer and fall.

Okay. And just one question on the Alzheimer disease program. Could you remind us what's the data set we could be expecting there later this year?

So remember, just a reminder, this is a Phase I trial in patients with inflammation and Alzheimer's disease. And so they had to have inflammation -- biomarkers of inflammation to be enrolled because remember, we're -- our hypothesis is that neuroinflammation is a cause of their disease. So they get treated for 3 months. And the primary readouts, the primary goal of the trial is to prove we get rid of neuroinflammation. The hypothesis is that if neuroinflammation causes nerve cell death and synaptic dysfunction, if we get rid of neuroinflammation, then we will improve -- decrease the amount of neuro cell death and synaptic dysfunction.

But to get a cognitive readout is going to take more than 3 months. So we are getting all that cognition assay -- or not assays, but measures, but that's not the primary endpoint. The primary endpoint is 4 different buckets. We have inflammatory and neurodegenerative biomarkers in blood and CSF, so cytokines, filaments. We're using the Roche neuro toolkit for these assays. So that's blood and CSF as a standard.

We are measure -- using MRI imaging to look at white-matter free water, which is an area that I am quite keen on. It turns out that neuroinflammation increases the amount of free water in the white matter, and you can measure that by MRI sequences. So that is a very attractive biomarker.

We are getting a breath test, looking at volatile organic compounds that are expressed in the breath, which is an excellent biomarker of inflammation. And then finally, we are looking at what we call the behavioral biomarkers. It turns out that depression, agitation, hallucinations, sleep disorders and apathy are common problems in Alzheimer's patients, and they are exquisitely sensitive to neuroinflammation.

So the assumption is -- or the hypothesis is that these will improve. So it's the suite of 5 biomarker buckets that we're looking at, and that is the -- those are the endpoints that we're going to use to move into Phase II.

Great. And just one maybe quick housekeeping question for David. So regarding the SG&A expense line, could you -- could we assume it goes flat over the rest of the year?

Yes. Yes, you can, Arthur.

At this time, I would like to turn the call back over to Mr. RJ Tesi for closing comments.

So we'd like to thank you all for joining us today. We are excited about the future. As you know, we have a full plate or a full slate of programs. We are working hard in these difficult times. We have prioritized our programs in a way that we think we can bring value to the company and to investors and to make a difference at the bedside.

So with that, I thank you all. David, anything you want to add?

No. I appreciate everybody's patience in what we're doing here, and I certainly appreciate everybody's support. And as with always, if you have questions, please reach out to us individually and independently, we'd be more than delighted to chat with you.

Thank you. This does conclude today's teleconference. You may disconnect your lines at this time, and have a great day.